We aimed to clarify the self-organizing mechanisms for the hierarchical multi-oscillator structure of the mammalian circadian clock in the suprachiasmatic nucleus (SCN) using knockout mice for clock genes and neuropeptides functions, luciferase reporter mice for continuous monitoring clock gene expression, and fluorescence sensors for monitoring intracellular calcium and membrane potentials. We demonstrated that both VIP and vasopressin act as synchronizers for cellular rhythms. We also found that their roles change depending on postnatal development, in which clock gene Cry is involved. We also found that GABA in the SCN acts not in cellular rhythm generation but in coherent neural rhythm output from the SCN to make the central circadian clock free of bursts. We further found that Per1 rhythms in the discrete areas in the SCN are involved in transferring photoperiodic signals to behavior rhythm output by changing the phase relations.